formazans and Streptococcal-Infections

Streptococcus pyogenes is a notorious human pathogen responsible for a wide array of infections. The ability of S. pyogenes to form biofilms is an innate property during the pathogenesis of invasive infections. From the eleven M serotypes tested: M56, M74, M100, M65, M89 and st38 formed dense biofilms in 48 h. The present study is the first of its kind to report about the biofilm formation in the serotypes M56, M65 M74 M100 and st38. XTT reduction assay of the biofilms showed decreased metabolic activity with increase in incubation time. The surface architecture of the biofilms when observed by scanning electron microscopy (SEM) revealed the microcolony formation. Confocal laser scanning microscopy (CLSM) was used to compare the surface topography and thickness of biofilms between the biofilm formers with and without the addition of glucose. Interestingly a non-biofilm former (st2147) was induced to form biofilms with the addition of glucose. On correlating the drug (erythromycin) resistance of the various M serotypes with their biofilm forming ability we noticed that erythromycin sensitive strains were found to be good biofilm formers. We also noticed that biofilm formation in S. pyogenes is independent of sil gene.

Topics: Adolescent; Anti-Bacterial Agents; Biofilms; Child; Child, Preschool; Drug Resistance, Bacterial; Erythromycin; Formazans; Glucose; Humans; Microscopy, Confocal; Microscopy, Electron, Scanning; Streptococcal Infections; Streptococcus pyogenes

The glossy non-encapsulated strain of Steptococcus equi, NCTC 9682, was compared with the matt strain Hidaka/95/2 which expresses a medium sized capsule and with the mucoid CF32 which expresses a large sized capsule in phagocytosis assays and for virulence in inoculated horses. The three strains, NCTC 9682, Hidaka /95/2 and CF32 produced 2.0, 3.1, and 5.3 mg/g wet cells respectively after 3 h incubation, but similar amounts of M-like proteins, cytotoxin and mitogen. NCTC 9682 showed no resistance to phagocytosis by equine neutrophils regardless of the presence of opsonin while strains Hidaka /95/2 and CF32 showed almost complete resistance to phagocytosis. Furthermore, NCTC 9682 produced no clinical disease although it infected the guttural pouch and caused seroconversion. Typical strangles with guttural pouch invasion was observed in all horses infected with encapsulated strains.

Topics: Animals; Antibodies, Bacterial; Bacterial Capsules; Blotting, Western; Carbazoles; Carbon; Colony Count, Microbial; Coloring Agents; Enzyme-Linked Immunosorbent Assay; Female; Formazans; Gene Expression Regulation, Bacterial; Horse Diseases; Horses; Hyaluronic Acid; Japan; Lymph Nodes; Palatine Tonsil; Phagocytosis; Streptococcal Infections; Streptococcus equi; Tetrazolium Salts; United States

The adherence of circulating phagocytes to glass was studied in 15 children with acute poststreptococcal glomerulonephritis and in 27 healthy adults, 21 healthy children, and 14 children with normocomplementemic renal disease. The phagocytic adherence to glass in the patients with hypocomplementemic PSGN differed significantly from that of the control groups (p=less than 0.001). There was a positive correlation of phagocyte adherence with plasma C3 but not with plasma C4, C3, properdin factor B, severity of illness, or drugs administered. In addition, the adherence defect was present in two normocomplementemic PSGN patients. The defect gradually resolved in all patients with clinical improvement: it was useful as an index of recovery. The in vitro addition of functional C3 to whole blood produced the adherence defect in normal subjects and failed to correct the defect in patients with PSGN. It was postulated that a fragment of activated complement may have blocked a membrane receptor on these phagocytes and interfered with their adherence to glass.

Topics: Adolescent; Adult; Antigen-Antibody Reactions; Child; Child, Preschool; Complement C3; Complement C4; Female; Formazans; Glomerulonephritis; Humans; In Vitro Techniques; Male; Phagocytes; Streptococcal Infections